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A subtype of receptor for dopamine involved in neural signalling and targeted by many antipsychotic medications. Receptor blockade is a pharmacological action, not a complete psychological description of treatment response.

Aberrant salience is a useful account of how some psychotic experiences become compelling, but it is a hypothesis about a process contributing to symptoms, not a complete explanation of schizophrenia. Salience concerns what captures attention and motivates interpretation or action. It is distinct from whether a stimulus is physically intense, pleasurable or objectively informative.

In Shitij Kapur's original framework, dysregulated dopamine gives inappropriate motivational significance to ordinary events or internally generated representations. A coincidental glance can consequently feel urgent and personally directed. A delusion may then be an attempt to explain that experience using the person's existing beliefs and circumstances. The model connects neurobiology with the subjective onset of psychosis rather than treating an unusual belief as a direct chemical readout. It also predicts that dampening salience can reduce the compelling quality of experiences before their interpretation has been revised. This is a theoretical synthesis, not an experiment proving the entire causal chain.^[ref]

The framework makes two separable predictions: inappropriate significance should attach to uninformative cues, and relevant cues may fail to gain appropriate significance. They should be measured independently. In the Salience Attribution Test used by Jonathan P. Roiser and colleagues, visual cues varied along colour and form dimensions, with only one dimension predicting monetary reinforcement. Reaction-time speeding and explicit probability ratings indexed responding to relevant versus irrelevant features. Patients showed reduced adaptive salience; importantly, the diagnostic groups did not differ overall in aberrant salience. Greater explicit aberrant salience occurred in patients with delusions relative to patients without them. The small, predominantly medicated sample, subgroup analysis and multiple comparisons prevent presenting this as a universal schizophrenia deficit.^[ref]

A useful measurement caution follows directly. If equally uninformative features receive noisy ratings $R_1,R_2$, the absolute difference $|R_1-R_2|$ is generally positive even when both estimates are unbiased. For independent normal errors of variance ${\sigma }^2$, its expectation is $2\sigma /\sqrt{\pi }$. A high score can therefore reflect rating noise or poor probability discrimination as well as genuinely assigned significance. Repeated trials, reliability assessment, explicit task comprehension and measurements of adaptive learning are needed to interpret the score.

Biological evidence is compatible with, but does not uniquely identify, the hypothesis. Oliver D. Howes and colleagues used fluorodopa PET to compare people with prodromal symptoms, patients with schizophrenia and controls. Elevated synthesis-related uptake in the associative striatum in the prodromal group links dopamine dysfunction to a stage before established psychotic illness. This was a case-control study; uptake is not a recording of cue-specific phasic dopamine, and a high-risk group does not establish that every individual will develop schizophrenia. It supplies an upstream biological constraint, not a demonstration that a particular neutral cue caused a delusion.^[ref]

Several explanatory steps remain. An account must specify why significance is assigned to this event, how a persistent interpretation is selected, and why contradictory evidence fails to revise it. Attention, memory retrieval, prior beliefs and the social environment can supply those constraints. Dopamine dysfunction need not explain all negative symptoms or cognitive difficulties. Antipsychotic effects cannot alone establish the original cause: altering a downstream component can improve symptoms arising through several pathways. Nor should a medication-associated decrease in ordinary motivation automatically be taken as recovery of selective salience.

A similar perspective is particularly productive for substance use disorder. Incentive salience distinguishes cue-triggered wanting from pleasure. Cindy L. Wyvell and colleagues separately trained a sucrose-seeking response and a reward-predictive cue. Accumbens amphetamine enhanced cue-triggered responding in a test without reward reinforcement, without enhancing sucrose liking measured by taste reactivity. A later sensitization experiment found amplified cue-triggered seeking in a drug-free test after prior exposure. The experiments distinguish motivation from hedonic impact; they do not themselves demonstrate every feature of human addiction.^[ref][ref]

This suggests how drug cues can capture behaviour even when enjoyment has declined or the person intends abstinence. Unlike psychosis, however, these cues were genuinely associated with reward. The shared issue is excessive or poorly regulated motivational control, not necessarily significance attached to statistically irrelevant events.

Anxiety disorders offer a second, more limited analogy: threat-related cues can monopolise attention, avoidance can maintain their significance, and safe cues may be treated as dangerous. In panic disorder, catastrophic interpretation can make ordinary bodily sensations feel threatening. Such accounts concern threat appraisal and discrimination and do not justify assuming identical dopamine abnormalities across diagnoses. Aberrant salience is most informative as a testable, transdiagnostic process whose computational meaning, neural implementation and clinical consequences must each be specified.

This combination warrants a grave prognosis and closely supervised treatment of both the pneumonia and the delirium tremens; recovery cannot be promised or ruled out from the diagnosis alone. The immediate conflict is that the agitation and sleeplessness of alcohol withdrawal call for effective control, while pneumonia reduces respiratory reserve. Excessive sedation can then worsen hypoventilation and aspiration, whereas uncontrolled delirium tremens can itself be life-threatening.

An historically reasoned 1864 approach would emphasise continuous nursing, a quiet environment, nourishment and fluids that the person could safely swallow, and repeated examination of the thorax and circulation. Suppressing a cough or inducing sleep would not demonstrate resolution of the pneumonia. The traditional strongly depleting approach to inflammation, including bloodletting and large doses of tartar emetic, would be especially hazardous in an exhausted person. Opium and alcoholic stimulation were debated contemporary remedies; escalating opium simply because sleep had not occurred could deepen respiratory depression. Period discussion of delirium tremens explicitly recognised that treatment response varied and that intercurrent disease altered the outlook.^[ref] These are historical treatment controversies, not present instructions to administer alcohol or opium.

Modern management is in hospital, with an appropriate level of observation and early critical-care assessment if breathing or consciousness deteriorates. Assess the airway, respiratory rate, oxygen saturation, blood pressure, temperature, blood glucose and electrolytes. Establish the severity and likely cause of the pneumonia, including possible aspiration; a chest radiograph and microbiological samples are used as indicated. Give timely antibiotics selected for the setting, severity, likely organisms and local resistance patterns. Provide oxygen therapy or more advanced respiratory support when indicated, while reassessing the response.^[ref]

Treat the delirium tremens using an appropriate benzodiazepine regimen with frequent reassessment; the respiratory illness makes skilled monitoring particularly important, rather than making untreated withdrawal acceptable. Provide thiamine, with the parenteral route when indicated by malnutrition or suspected Wernicke encephalopathy, and correct relevant deficiencies. Hypoglycaemia requires prompt treatment. Antipsychotics are not a replacement for treatment of the underlying alcohol withdrawal.^[ref]

Historically the absence of effective antibiotics made the additional pneumonia particularly ominous. Today the outlook depends on respiratory failure, sepsis, coexisting organ disease and treatment response. No severity findings, age or organ-function results are supplied, so neither a mortality percentage nor an inevitable fatal outcome follows. A poor result would also not, by itself, prove that a particular historical remedy caused or prevented death.

Historical “acute mania” in women must be separated into a manic syndrome, psychosis associated with childbirth and disturbed behaviour caused by physical disease or drugs. Reproductive events can be clinically relevant without making female anatomy a sufficient explanation for mental illness.

A typical manic episode involves a marked change from the person's usual state: elevated or irritable mood, increased activity, little felt need for sleep, rapid or pressured speech, distractibility, impulsive decisions and exaggerated confidence. Severe illness can include delusions, hallucinations, disorganization and dangerous loss of judgement. Physical exhaustion or failure to eat can follow sustained activity. These are possible features of the syndrome, not assertions about an unspecified woman.^[ref] Fluctuating attention, disorientation, fever or a changing level of consciousness instead prompts particular concern for delirium and its cause.

In an 1866 account, chief associations would include the puerperal period, prolonged nursing with exhaustion, previous attacks, family predisposition, severe emotional disturbance and general illness. Historical “puerperal insanity” also included depressive and psychotic presentations, not just what is now called bipolar disorder. A contemporary journal summary distinguished pregnancy, puerperal and lactational groups and noted hereditary associations, recurrence and suicidal behaviour. Its observed associations do not establish menstrual suppression or nursing itself as a single sufficient cause.^[ref]

The practical historical aims were protection from injury, restoration of sleep and nutrition, a calm environment, attentive nursing and treatment of physical illness. Someone unable to care safely for herself or an infant required continuous help. Opiates, baths and other sedating measures were tried; quietness after sedation did not prove cure. Depleting a person already exhausted by childbirth or blood loss could worsen the illness. Neither punishment nor treatment of an assumed uterine defect addresses a properly established mental disorder.

Modern correction: assess risk and distinguish primary psychiatric illness from a medical emergency. Consider bipolar disorder, medication- or substance-related illness, thyroid disease, neurological disease and infection. After childbirth, distinguish postpartum psychosis from delirium due to sepsis, metabolic disturbance or another obstetric complication. Protect the woman and baby while arranging prompt specialist assessment. NICE recommends immediate assessment, within four hours of referral, for sudden symptoms suggesting postpartum psychosis.^[ref]

For established mania, current treatment may include an appropriate antipsychotic, specialist use of a mood stabilizer, and review of medicines such as an antidepressant that may be contributing. Pregnancy, breastfeeding, previous treatment response, physical disease and monitoring requirements affect the choice. In severe or treatment-resistant illness, additional specialist interventions may be needed. Treat delirium by addressing its physical cause alongside safe supportive care; it is not interchangeable with a manic episode.^[ref][ref] The organizing principle is a diagnosis and a safe care plan, not a presumption that all acute behavioural change in a woman is “uterine mania”.

Risperidone is an antipsychotic with antagonistic actions at dopamine D2 receptors and serotonin receptors. These interactions are part of its pharmacology, while its complete mechanism of clinical benefit remains incompletely established.^[ref]